scholarly journals Pulmonary hypertension. Clarifying concepts

ANALES RANM ◽  
2021 ◽  
Vol 138 (138(02)) ◽  
pp. 137-142
Author(s):  
J.R. de Berrazueta Fernández
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Structural Changes ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Current Classification ◽  
Mean Pressure ◽  
Pulmonary Arterial ◽  
The Difference

Pulmonary Arterial Hypertension is a central syndrome produced by a large number of cardiological, pulmonary, and systemic diseases that affect the lung bed. It is defined by the existence of a pulmonary artery systolic pressure greater than 30 or a mean pressure greater than 25 mmHg. This definition criterion has been maintained for more than 60 years. However, the current classification includes two concepts: a Pulmonary Arterial Hypertension (PAH) with two groups of disorders in which only pulmonary arterial resistance increases and five groups that are classified as Pulmonary Hypertension (PH): PH Secondary to Pulmonary Veno-occlusive Disease , HP secondary to diseases of the left side of the heart; HP Obliterative diseases and pulmonary hypoxemia; HP Pulmonary thrombus occlusive diseases, and a group of multifactorial HP. The difference is found in how the different diseases affect the pulmonary vascular bed, and how they alter the physiology or behavior of pulmonary resistance, which are the concepts that must be handled when talking about this syndrome and whose structural changes and management we will discuss in a later article.

scholarly journals The Effects of Dexmedetomidine Prescription in Paediatric Patients With Pulmonary Hypertension Under Congenital Heart Surgery

2020 ◽  
Author(s):  
Bahram Ghasemzadeh ◽  
Bahador Azizi ◽  
Simin Azemati ◽  
Mostafa Bagherinasab
Keyword(s):  
Blood Pressure ◽  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Systolic Blood Pressure ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Anesthetic Care ◽  
Pulmonary Arterial

Anesthetized patient management for pediatric patients with pulmonary arterial hypertension (PAH) is a major challenge. The aim of this study was to evaluate the ability of dexmedetomidine to reduce pulmonary arterial hypertension in patients with pulmonary arterial hypertension undergoing cardiac surgery. Sixty-six patients with pulmonary arterial hypertension underwent the study. Patients were randomly divided into two groups: group D received a dexmedetomidine injection in a dose of 1 μg/kg in the first hour and then decreased to 0.5 μg/kg/hr, injection continued after surgery until extubation in the post-anesthetic care unit (PACU). Group C received normal saline 0.9% in a similar volume. Pulmonary artery systolic pressure (PASP) and systemic systolic blood pressure (SSBP) were recorded during and after the surgery in the postanesthetic care unit. Needing vasodilators, sedatives, extubation time, and the length of ICU stay were recorded for all patients. Patients in the dexmedetomidine group showed a significant reduction in Pulmonary artery systolic pressure and Pulmonary artery systolic pressure/systemic systolic blood pressure rates during surgery and during the first 24 hours in the post-anesthetic care unit (P<0.001). The dexmedetomidine group, in comparison with the control group, needed a significantly lower dose of a vasodilator (P<0.001) and a lower dose of sedation (P<0.001). It is concluded that the use of dexmedetomidine during the surgery in children with pulmonary hypertension reduces pulmonary artery systolic pressure during and after the surgery.

scholarly journals Pulmonary hypertension: reasonable selection of specific therapy

2018 ◽  
Vol 15 (1) ◽  
pp. 45-50
Author(s):  
N A Karoli ◽  
S I Sazhnova ◽  
A P Rebrov
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Structural Changes ◽  
Pulmonary Arteries ◽  
Endothelin Receptor Antagonists ◽  
Endothelin Receptor ◽  
Receptor Antagonists ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial

Pulmonary hypertension is characterized with persistent increase in pulmonary vascular resistance leading to progressive worsening of right ventricular failure and death. The basis for pulmonary arterial hypertension is structural changes in pulmonary arteries and arterioles caused by endothelial dysfunction. Endothelin-1 is the main pathogenic trigger of pulmonary hypertension and potential target for therapeutic exposure. The efficacy of endothelin receptor antagonists is proved in various preclinical and clinical studies. In patients with pulmonary arterial hypertension, the efficacy of dual and selective endothelin receptor antagonists is comparable despite the varied activity against various receptors. Bosentan is the most widely used pulmonary vasodilator which improves exercise tolerance and decelerates disease progression.

scholarly journals Pneumonectomy combined with SU5416 induces severe pulmonary hypertension in rats

2016 ◽  
Vol 310 (11) ◽  
pp. L1088-L1097 ◽  
Author(s):  
C. M. Happé ◽  
M. A. de Raaf ◽  
N. Rol ◽  
I. Schalij ◽  
A. Vonk-Noordegraaf ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Systolic Pressure ◽  
Endothelial Cell Proliferation ◽  
Pulmonary Vasculature ◽  
Hypoxic Exposure ◽  
Sprague Dawley ◽  
Pulmonary Arterial ◽  
Severe Pulmonary Arterial Hypertension

The SU5416 + hypoxia (SuHx) rat model is a commonly used model of severe pulmonary arterial hypertension. While it is known that exposure to hypoxia can be replaced by another type of hit (e.g., ovalbumin sensitization) it is unknown whether abnormal pulmonary blood flow (PBF), which has long been known to invoke pathological changes in the pulmonary vasculature, can replace the hypoxic exposure. Here we studied if a combination of SU5416 administration combined with pneumonectomy (PNx), to induce abnormal PBF in the contralateral lung, is sufficient to induce severe pulmonary arterial hypertension (PAH) in rats. Sprague Dawley rats were subjected to SuPNx protocol (SU5416 + combined with left pneumonectomy) or standard SuHx protocol, and comparisons between models were made at week 2 and 6 postinitiation. Both SuHx and SuPNx models displayed extensive obliterative vascular remodeling leading to an increased right ventricular systolic pressure at week 6. Similar inflammatory response in the lung vasculature of both models was observed alongside increased endothelial cell proliferation and apoptosis. This study describes the SuPNx model, which features severe PAH at 6 wk and could serve as an alternative to the SuHx model. Our study, together with previous studies on experimental models of pulmonary hypertension, shows that the typical histopathological findings of PAH, including obliterative lesions, inflammation, increased cell turnover, and ongoing apoptosis, represent a final common pathway of a disease that can evolve as a consequence of a variety of insults to the lung vasculature.

scholarly journals EXPRESS: Pulmonary arterial hypertension in pregnancy – a systematic review of outcomes in the modern era

2021 ◽  
pp. 204589402110136
Author(s):  
Ting Ting Low ◽  
Nita Guron ◽  
Robin Ducas ◽  
Kenichiro Yamamura ◽  
Pradeepkumar Charla ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Mortality Rate ◽  
Arterial Hypertension ◽  
Maternal Mortality ◽  
Post Partum ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Maternal Mortality Rate ◽  
Pulmonary Arterial ◽  
In Pregnancy

Background: Pregnancy is hazardous with pulmonary arterial hypertension (PAH), but the risks may have improved in recent years. We sought to systematically evaluate PAH and pregnancy-related outcomes in the last decade. Methods: We searched for articles describing outcomes in pregnancy cohorts published between 2008-2018. 3658 titles were screened and 13 studies included for analysis. Pooled incidences and percentages of maternal and perinatal outcomes were calculated.  Results: Out of 272 pregnancies, 214 pregnancies advanced beyond 20 gestational weeks. The mean maternal age was 28±2 years, mean pulmonary artery systolic pressure on echocardiogram was 76±19mmHg. Aetiologies include idiopathic PAH 22%, congenital heart disease 64%, and others 15%. Majority (74%) had good functional class I/II. Only 48% of women received PAH-specific therapy. Premature deliveries occur in 58% of pregnancies at mean of 34±1 weeks, most (76%) had caesarean section. Maternal mortality rate was 12% overall (n=26); even higher for idiopathic PAH aetiology alone (20%). Reported causes of death included right heart failure, cardiac arrest, PAH crises, pre-eclampsia and sepsis. 61% of maternal deaths occur at 0-4 days post-partum. Stillbirths rate was 3% and neonatal mortality rate 1%. Conclusions: PAH in pregnancy continues to be perilous with high maternal mortality rate. Continued prospective studies are needed.

scholarly journals Stable Gastric Pentadecapeptide BPC 157 Therapy for Monocrotaline-Induced Pulmonary Hypertension in Rats Leads to Prevention and Reversal

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 822
Author(s):  
Mario Udovicic ◽  
Marko Sever ◽  
Lovro Kavur ◽  
Kristina Loncaric ◽  
Ivan Barisic ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Systolic Pressure ◽  
Bodyweight Loss ◽  
Novel Therapy ◽  
Bpc 157 ◽  
Qt Interval Prolongation ◽  
Pentadecapeptide Bpc 157 ◽  
Pulmonary Arterial

Background. Monocrotaline selectively injures the lung’s vascular endothelium and induces pulmonary arterial hypertension. The stable gastric pentadecapeptide BPC 157 acts as a prototype cytoprotective agent that maintains endothelium, and its application may be a novel therapy. Besides, BPC 157 prevents and reverses thrombosis formation, maintains platelet function, alleviates peripheral vascular occlusion disturbances, and has anti-arrhythmic and anti-inflammatory effects. Monocrotaline-induced pulmonary arterial hypertension in rats (wall thickness, total vessel area, heart frequency, QRS axis deviation, QT interval prolongation, increase in right ventricle systolic pressure and bodyweight loss) can be counteracted with early or delayed BPC 157 therapy. Methods and Results. After monocrotaline (80 mg/kg subcutaneously), BPC 157 (10 μg/kg or 10 ng/kg, days 1–14 or days 1–30 (early regimens), or days 14–30 (delayed regimen)) was given once daily intraperitoneally (last application 24 h before sacrifice) or continuously in drinking water until sacrifice (day 14 or 30). Without therapy, the outcome was the full monocrotaline syndrome, marked by right-side heart hypertrophy and massive thickening of the precapillary artery’s smooth muscle layer, clinical deterioration, and sometimes death due to pulmonary hypertension and right-heart failure during the 4th week after monocrotaline injection. With all BPC 157 regimens, monocrotaline-induced pulmonary arterial hypertension (including all disturbed parameters) was counteracted, and consistent beneficial effects were documented during the whole course of the disease. Pulmonary hypertension was not even developed (early regimens) as quickly as the advanced pulmonary hypertension was rapidly attenuated and then completely eliminated (delayed regimen). Conclusions. Thus, pentadecapeptide BPC 157 prevents and counteracts monocrotaline-induced pulmonary arterial hypertension and cor pulmonale in rats.

scholarly journals Docosahexaenoic acid causes rapid pulmonary arterial relaxation via KCa channel-mediated hyperpolarisation in pulmonary hypertension

2016 ◽  
Vol 48 (4) ◽  
pp. 1127-1136 ◽  
Author(s):  
Chandran Nagaraj ◽  
Bi Tang ◽  
Bence M. Nagy ◽  
Rita Papp ◽  
Pritesh P. Jain ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Membrane Potential ◽  
Pulmonary Arterial Hypertension ◽  
Docosahexaenoic Acid ◽  
Arterial Hypertension ◽  
Vascular Tone ◽  
Systolic Pressure ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
Kca Channels ◽  
Pulmonary Arterial

Cardioprotective benefits of ω-3 fatty acids such as docosahexaenoic acid (DHA) are well established, but the regulatory effect of DHA on vascular tone and pressure in pulmonary hypertension is largely unknown.As DHA is a potent regulator of K+ channels, we hypothesised that DHA modulates the membrane potential of pulmonary artery smooth muscle cells (PASMCs) through K+ channels and thus exerts its effects on pulmonary vascular tone and pressure.We show that DHA caused dose-dependent activation of the calcium-activated K+ (KCa) current in primary human PASMCs and endothelium-dependent relaxation of pulmonary arteries. This vasodilation was significantly diminished in KCa–/– (Kcnma1–/–) mice. In vivo, acute DHA returned the right ventricular systolic pressure in the chronic hypoxia-induced pulmonary hypertension animal model to the level of normoxic animals. Interestingly, in idiopathic pulmonary arterial hypertension the KCa channels and their subunits were upregulated. DHA activated KCa channels in these human PASMCs and hyperpolarised the membrane potential of the idiopathic pulmonary arterial hypertension PASMCs to that of the PASMCs from healthy donors.Our findings indicate that DHA activates PASMC KCa channels leading to vasorelaxation in pulmonary hypertension. This effect might provide a molecular explanation for the previously undescribed role of DHA as an acute vasodilator in pulmonary hypertension.

scholarly journals Dynamics of the clinical functional and hemodynamic profile of patients with pulmonary arterial hypertension with initial monotherapy with endothelin receptor antagonists: bosentan vs. macitentan

Kardiologiia ◽  
2020 ◽  
Vol 60 (7) ◽  
pp. 28-35
Author(s):  
T. V. Martynyuk ◽  
A. M. Aleevskaya
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Treatment Group ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Eisenmenger Syndrome ◽  
Pulmonary Hemodynamics ◽  
Cardiothoracic Ratio ◽  
Pulmonary Arterial

Aim To compare results of 24-h treatments with bosentan and macitentan by the clinical functional status and indexes of pulmonary hemodynamics in patients with pulmonary arterial hypertension (PAH).Materials and methods Based on the Russian National Registry (NCT03707561), 44 patients older than 18 years with PAH (34 patients with idiopathic pulmonary hypertension (IPH) and 10 patients with Eisenmenger syndrome) were retrospectively included into this study. Based on the statistical method of pairwise comparison, two groups were formed and matched by age, gender, WHO functional class (FC), and 6-min walk distance (6MWD). 22 patients of group 1 (17 with IPH and 5 with Eisenmenger syndrome) were treated with macitentan 10 mg/day, and 22 patients of group 2 (17 with IPH and 5 with Eisenmenger syndrome) were treated with bosentan 250 mg/day. Clinical instrumental data (6MWD, Borg dyspnea score, chest X-ray, transthoracic echocardiography (EchoCG), and right heart catheterization (RHC)) were evaluated at baseline and after 24 weeks of therapy.Results By week 24 of the treatment, FC and 6MWD improved in both groups. The macitentan treatment was associated with a significant decrease in Borg score. Significant intergroup differences in EchoCG data were not observed. The bosentan treatment was associated with a decrease in right ventricular (RV) dimension and a tendency towards a decrease in calculated pulmonary artery systolic pressure (PASP). By week 24, the macitentan treatment as compared to the bosentan treatment, was associated with a decrease in cardiothoracic ratio (CTR). In both groups, RHC showed decreases in PASP, mean pulmonary artery pressure and pulmonary vascular resistance, and improvements in cardiac output (CO), cardiac index, and stroke volume (SV) values. By week 24, the increase in SV was greater in the macitentan treatment group than in the bosentan treatment group (р=0.05).Conclusion The 24-week treatment with bosentan or macitentan provided significant and comparable improvement of the functional profile in PAH patients with FC II (WHO) at baseline. The decrease in CTR was significantly more pronounced in the macitental treatment group compared to the bosentan treatment group. The 24-week bosentan treatment resulted in a decrease in RV anterior-posterior dimension, a tendency towards a decrease in PASP according to EchoCG data. Macitentan provided more pronounced dynamics of dyspnea than bosentan according to the results of 6MWD test and the increase in SV according to RHC data.

scholarly journals Evaluation of effectiveness and safety of the first Russian-manufactured generic bosentan use in patients with pulmonary arterial hypertension

2018 ◽  
Vol 15 (4) ◽  
pp. 53-58
Author(s):  
O A Arkhipova ◽  
S E Gratsianskaya ◽  
T V Martynyuk
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Pulmonary Artery Systolic Pressure ◽  
Heart Catheterization ◽  
Walk Distance ◽  
Pulmonary Arterial ◽  
Minute Walk Distance ◽  
Minute Walk

Objective. To study effectiveness and safety of generic bosentan use for 24 weeks in patients with pulmonary arterial hypertension (PAH). Materials and methods. The study included 42 patients. In 22 patients Bosentan therapy (Bosenex®, Sotex, Russia) was used for the first time. In 20 patients switching therapy from original bosentan (Tracleer, Аctelion Pharmaceuticals Ltd., Switzerland) was performed. The patients were followed up for 24±2 weeks. Results. After 24 weeks of treatment percent of patients with functional class (FC) III decreased from 55 to 30%, percent of patients with FC II increased from 45 to 55%, some patients (15%) achieved FC I, and the 6-minute walk distance increased on 52.1 meters. In the group of therapy change heart failure FC stabilization was observed, 6-minute walk distance increased on +14.8 meters (р>0.05). Echocardiography in the first group showed significant decrease of pulmonary artery systolic pressure (PASP) at -4 mm Hg and of right atrium area on 0.9 cm2. In the switched therapy group the difference was not significant. According to chest X-ray examination change of cardio-thoracic ratio, Murray and Lupi indexes was not significant in both groups. According to results of right heart catheterization improvement of mean pulmonary arterial pressure (-6.7 mm Hg), mean right atrial pressure (-1.6 mm Hg with reference value reached), and pulmonary vascular resistance (-293.2 dynes×sec/cm-5) was achieved; р

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